engleski

Treatment of postoperative hypocalcemia

Postoperative hypocalcemia is one of the most com¬ ; mon complications of thyroid surgery. It is related to the type of disease (malignant or benign), number of par¬ ; athyroid glands identified during surgical procedure, re-operation and the surgeon's experience. Postoperative hypoparathyroidism can be temporary or permanent. The incidence of permanent hypoparath¬ ; yroidism has been reported to range from as high as more than 20%, when total thyroidectomy and radical neck dissection are performed, to as low as 0.9% ; however, there are reports on an even lower incidence of perma¬ ; nent hypoparathyroidism. Operative strategies to prevent postoperative hy¬ ; poparathyroidism include preservation of parathyroid glands in situ and autotransplantation of parathyroid glands during total thyroidectomy. Postoperative hypoparathyroidism results in hypoc¬ ; alcemia, hyperphosphatemia, and low parathyroid hor¬ ; mone (PTH) level. Intraoperative PTH at 20 to 30 min¬ ; utes after total thyroidectomy can predict impending postoperative hypocalcemia. Acute hypocalcemia directly causes increased neu- romuscular irritability, and this pathophysiology under¬ ; lies the most prominent symptoms. Tetany is seen in more severe hypocalcemia. If there is any doubt, the presence of hypocalcemia needs to be confirmed by the measurement of serum ionized calcium. The diagnosis is confirmed by a find¬ ; ing of serum calcium <2.05 mmol/L or ionized calcium <1.1 mmol/L. Patients with acute symptomatic hypocalcemia (se¬ ; rum calcium <0.8 mmol/L) should be treated promptly with IV calcium. Calcium gluconate is preferred to calci¬ ; um chloride because it causes less tissue necrosis if ex-travasated. The first 100 to 200 mg of elemental calcium (1 to 2 g calcium gluconate) should be given over 10 to 20 minutes. Faster administration may result in cardiac dys¬ ; function, or even arrest. This should be followed by slow calcium infusion at 0.5 to 1.5 mg/kg/h. Calcium infusion should be continued until the patient can receive effec¬ ; tive doses of oral calcium and vitamin D. Chronic hypocalcemia is treated by the administra¬ ; tion of oral calcium and, if it is insufficient, vitamin D supplementation (0.25 to 0.50 mg of 1, 25-(OH) vita¬ ; min D is the usual initial daily dose). Appropriate doses of calcium and vitamin D are established by gradual ti-tration. The serum calcium level should be targeted to about 2.0 mmol/L. Most patients will be entirely asymp¬ ; tomatic at this level, and further elevation will lead to hypercalciuria because of the lack of PTH effect on the renal tubules. Chronic hypercalciuria may lead to the development of nephrocalcinosis, nephrolithiasis, renal impairment, and should be avoided. With the recent availability of synthetic PTH prep¬ ; arations (1- 34 PTH, teriparatide), several reports have described successful control of hypocalcemia with a low¬ ; er risk of hypercalciuria using twice- daily subcutaneous administration.

postoperative hypocalcemia ; thyroid surgery

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